Trekking guide at 4,850 m: AMS or HACE?
A 27-year-old trekking guide from Besisahar has crossed Thorong La (5,416 m) eleven times, but this season he stops at High Camp (4,850 m) with a throbbing bitemporal headache that began six hours ago, nausea, and breathlessness at rest. He is alert but slow to answer, and he stumbles twice on the heel-to-toe walk. He has a dry cough, his chest is clear, and there is no fever or chest pain. Pulse oximetry reads 71% on room air, pulse 106/min, respiratory rate 26/min. He forgot his acetazolamide at the last lodge, and he refuses to descend tonight: the group has already paid for the permit and the nearest lodge is six hours away over ice. The lodge owner offers bottled oxygen and the group's emergency supply of dexamethasone. The group leader asks you, the only person with first-aid training, to decide what should happen before morning.
1. Classify his illness using the Lake Louise criteria, and explain why the heel-to-toe finding matters more than the oximeter reading.
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Classification. Acute mountain sickness (AMS) requires headache plus at least one of: nausea/vomiting, fatigue or weakness, dizziness, or difficulty sleeping. He has headache plus nausea, so he meets the AMS criteria. But he also has ataxia on the heel-to-toe walk in a patient with AMS - by Lake Louise scoring this is high-altitude cerebral oedema (HACE) until proven otherwise, regardless of the headache score.
Why ataxia outranks the SpO2. Oximetry at altitude is a poor discriminator: healthy trekkers at 4,850 m routinely sit at 75–85%, and readings vary with cold fingers, perfusion and meter quality. A value of 71% is abnormal but not diagnostic on its own. Ataxia, by contrast, is a functional sign of a swollen brain; it is objective, reproducible and predicts death if untreated. Slow answering is a second red flag for altered mental status.
The dry cough with a clear chest does not yet prove HAPE, but it means he must be watched for it - HAPE and HACE frequently coexist.
2. Explain the acid–base change at this altitude and the mechanism by which acetazolamide would alter it.
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What altitude does. At 4,850 m the barometric pressure is roughly half that at sea level, so the inspired oxygen pressure is halved. The carotid bodies detect the fall in arterial PO2 and drive ventilation up. Alveolar and arterial PCO2 fall (typically to 25–30 mmHg), producing respiratory alkalosis.
Why the body then limits itself. The high pH of blood and, more importantly, of cerebrospinal fluid reduces the firing of central chemoreceptors, so the hyperventilation is partly braked - a trade-off that protects pH but lowers alveolar PO2 further. Over two to four days the kidney compensates by excreting bicarbonate, allowing ventilation to rise again.
What acetazolamide does. It inhibits carbonic anhydrase in the proximal tubule, causing bicarbonate diuresis and a mild metabolic acidosis that restores the hypoxic ventilatory drive. It also inhibits carbonic anhydrase in the choroid plexus, reducing CSF formation and making CSF slightly more acidic, which further stimulates breathing. It also causes paraesthesia, a metallic taste and diuresis. It is prophylaxis and adjunctive therapy - never a substitute for descent in HACE.
3. Rank descent, oxygen and dexamethasone for this patient and justify the order. What would you do if descent tonight is genuinely unsafe?
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Ranking.
- Descent of 500–1,000 m is definitive: it removes the hypobaric hypoxia that is driving the oedema, and the benefit is immediate and independent of drugs.
- Dexamethasone treats the cerebral oedema itself (8 mg immediately, then 4 mg every 6 hours). It buys time but masks symptoms, so it must not be used to justify staying higher.
- Oxygen (target SpO2 >90%) is temporising; it helps but does not reverse the causal pressure problem.
If descent is unsafe tonight. Do not let him sleep unobserved. Give oxygen continuously, start dexamethasone, keep him warm and hydrated, use a portable hyperbaric chamber if available, and descend at first light. He must not walk unassisted.
What not to do. Nifedipine is for HAPE, not HACE, and is not indicated here. Acetazolamide alone is inadequate treatment for HACE. The permit cost is irrelevant to the decision - untreated HACE has a high mortality within hours.